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GWAS Study

The genetics of hemoglobin A2 regulation in sickle cell anemia.

Griffin PJ, Sebastiani P, Edward H et al.

25042611 PubMed ID
GWAS Study Type
1189 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

GP
Griffin PJ
SP
Sebastiani P
EH
Edward H
BC
Baldwin CT
GM
Gladwin MT
GV
Gordeuk VR
CD
Chui DH
SM
Steinberg MH
Chapter II

Abstract

Summary of the research findings

Hemoglobin A2 , a tetramer of α- and δ-globin chains, comprises less than 3% of total hemoglobin in normal adults. In northern Europeans, single nucleotide polymorphisms (SNPs) in the HBS1L-MYB locus on chromosome 6q and the HBB cluster on chromosome 11p were associated with HbA2 levels. We examined the genetic basis of HbA2 variability in sickle cell anemia using genome-wide association studies. HbA2 levels were associated with SNPs in the HBS1L-MYB interval and SNPs in BCL11A. These effects are mediated by the association of these loci with γ-globin gene expression and fetal hemoglobin (HbF) levels. The association of polymorphisms downstream of the β-globin gene (HBB) cluster on chromosome 11 with HbA2 was not mediated by HbF. In sickle cell anemia, levels of HbA2 appear to be modulated by trans-acting genes that affect HBG expression and perhaps also elements within the β-globin gene cluster. HbA2 is expressed pancellularly and can inhibit HbS polymerization. It remains to be seen if genetic regulators of HbA2 can be exploited for therapeutic purposes.

618 African American cases

Chapter III

Study Statistics

Key metrics and study information

1189
Total Participants
GWAS
Study Type
Yes
Replicated
173 African American cases, 398 Chinese ancestry individuals
Replication Participants
African American or Afro-Caribbean, East Asian
Ancestry
U.S.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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